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PPAR Could Contribute to the Pathogenesis of Hepatocellular Carcinoma

Viral hepatitis with hepatitis C virus or hepatitis B virus and chronic liver disease such as alcoholic or nonalcoholic steatohepatitis are critical factors in the development of hepatocellular carcinoma (HCC). Furthermore, diabetes is known as an independent risk factor for HCC. Peroxisome prolifer...

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Detalles Bibliográficos
Autores principales: Kimura, Osamu, Kondo, Yasuteru, Shimosegawa, Tooru
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Hindawi Publishing Corporation 2012
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3533465/
https://www.ncbi.nlm.nih.gov/pubmed/23316217
http://dx.doi.org/10.1155/2012/574180
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author Kimura, Osamu
Kondo, Yasuteru
Shimosegawa, Tooru
author_facet Kimura, Osamu
Kondo, Yasuteru
Shimosegawa, Tooru
author_sort Kimura, Osamu
collection PubMed
description Viral hepatitis with hepatitis C virus or hepatitis B virus and chronic liver disease such as alcoholic or nonalcoholic steatohepatitis are critical factors in the development of hepatocellular carcinoma (HCC). Furthermore, diabetes is known as an independent risk factor for HCC. Peroxisome proliferator-activated receptor (PPAR) is known to have an important role in fatty liver, and the mechanism of carcinogenesis has been clarified. PPAR controls ligand-dependent transcription, and three subtypes (α, δ, and γ) in humans are known. PPARs could contribute to the mechanisms of cell cycling, anti-inflammatory responses, and apoptosis. Therefore, to clarify the pathogenesis of HCC, we should examine PPAR signaling. In this paper, we have summarized the relevance of PPARs to the pathogenesis of HCC and cancer stem cells and possible therapeutic options through modifying PPAR signaling.
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spelling pubmed-35334652013-01-11 PPAR Could Contribute to the Pathogenesis of Hepatocellular Carcinoma Kimura, Osamu Kondo, Yasuteru Shimosegawa, Tooru PPAR Res Review Article Viral hepatitis with hepatitis C virus or hepatitis B virus and chronic liver disease such as alcoholic or nonalcoholic steatohepatitis are critical factors in the development of hepatocellular carcinoma (HCC). Furthermore, diabetes is known as an independent risk factor for HCC. Peroxisome proliferator-activated receptor (PPAR) is known to have an important role in fatty liver, and the mechanism of carcinogenesis has been clarified. PPAR controls ligand-dependent transcription, and three subtypes (α, δ, and γ) in humans are known. PPARs could contribute to the mechanisms of cell cycling, anti-inflammatory responses, and apoptosis. Therefore, to clarify the pathogenesis of HCC, we should examine PPAR signaling. In this paper, we have summarized the relevance of PPARs to the pathogenesis of HCC and cancer stem cells and possible therapeutic options through modifying PPAR signaling. Hindawi Publishing Corporation 2012 2012-12-16 /pmc/articles/PMC3533465/ /pubmed/23316217 http://dx.doi.org/10.1155/2012/574180 Text en Copyright © 2012 Osamu Kimura et al. https://creativecommons.org/licenses/by/3.0/ This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Review Article
Kimura, Osamu
Kondo, Yasuteru
Shimosegawa, Tooru
PPAR Could Contribute to the Pathogenesis of Hepatocellular Carcinoma
title PPAR Could Contribute to the Pathogenesis of Hepatocellular Carcinoma
title_full PPAR Could Contribute to the Pathogenesis of Hepatocellular Carcinoma
title_fullStr PPAR Could Contribute to the Pathogenesis of Hepatocellular Carcinoma
title_full_unstemmed PPAR Could Contribute to the Pathogenesis of Hepatocellular Carcinoma
title_short PPAR Could Contribute to the Pathogenesis of Hepatocellular Carcinoma
title_sort ppar could contribute to the pathogenesis of hepatocellular carcinoma
topic Review Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3533465/
https://www.ncbi.nlm.nih.gov/pubmed/23316217
http://dx.doi.org/10.1155/2012/574180
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